Six common beliefs addressed, Part 70

1. You need carbohydrates to build muscle.

No. Only protein builds muscle.

2. The "fast/feast cycle" will protect you from muscle loss.

The "fast/feast cycle" is a marketing term and it protects you from nothing.

There is no “fast/feast cycle”. You are either eating or not eating and there’s no mysterious “cycle” involved in it. The body knows how to recognize anabolic/catabolic states, through nutrient availability. It does this every night, as you sleep. 

This has nothing to do with "protection" from muscle loss, as the person with metabolic syndrome/diabetes is exceptionally good at muscle breakdown, since these are conditions of adaptation to starvation. Eating again after a short fast, allows muscle mass to grow, but long fasts diminish it again and you never grow as much as you lose, so you don’t even break even. You know what grows exceptionally well, when you eat after a long fast? Fat. You grow fat mass very, very well.

It’s very simple - Fast for a short duration and there’s no muscle loss. Fast for a long duration and there’s always muscle loss. This is not unknown. This is a well documented fact. It’s one of those rare facts that has actually been seen consistently in experiments. So no, the magical “fast/feast cycle”, whatever that is, will not save your muscle mass, it will only spare your fat mass.

3. Is there a cure for fatty liver disease?

Fortunately, fatty liver disease is much easier to treat than diabetes. The only known method of reversal, which does not require a liver transplant, is a very low carb/ketogenic style diet.

4. Is there anything that can be done about excessive hunger after a fast?

Yes. Shorten your fast, until that doesn’t occur.

Excessive hunger after fasting, while still obese, is a sign of active obesity. The body is making you eat more in order to increase fat storage. This is specifically triggered by fasting for long periods. There is no metabolic advantage to going hungry.

5. Hyperinsulinemia is the main driver of obesity.

It’s one of the drivers of obesity. The main driver is your entire neuroendocrine system. Remember insulin is not an obesity hormone, but it’s necessary to grow fat. Being hyperinsulinemic simply means that you are in a hormonal state, which is powerfully contributing to your obesity. Remove the hyperinsulinemia and you greatly improve your chances of controlling and reversing obesity. It’s actually the simplest obesogenic driver to take control of, as it responds to dietary changes relatively quickly and well.

But, it’s certainly not the main driver, nor is it the only driver. There are many drivers in obesity and that’s why you have to focus on an anti-obesity lifestyle, which addresses all drivers.

6. Hyperinsulinemia is the same as insulin resistance.

Hyperinsulinemia (HI) is a direct result of a high insulin demand on the body. This high insulin demand is being driven primarily by a combination of four things:

• Too much glucose in - The body must handle the tsunami of glucose that’s coming in from the diet, by raising insulin levels to disperse it out of the blood.
• Too much glucose out - The body is producing an enormous amount of glucose from itself, through the breakdown of lean muscle mass, which further stimulates insulin release from chronically high blood glucose.
• Too much fat in - Any dietary fat that is not burned, is stored and the storage of fat requires insulin. This raises basal insulin, further contributing to blood glucose dysregulation. 
  
• Too much body fat - The body requires a high basal insulin level to keep fat in storage, as that fat cannot be released into the bloodstream. Insulin is like a dam, keeping body fat in place, and this is actually where the bulk of high basal insulin is coming from. 

All of this leads to insulin resistance (IR) of certain organs and tissues, but not of the fat mass. If the fat mass became insulin resistant, it could not hold all that fat inside, nor store more of it. So, the fat mass requires high insulin sensitivity.

So, when people group all of these effects together and simply describe them as “Mah’ bad insulin resistance”, they are not truly understanding insulin’s effect on the body. Yes, it’s IR and HI, but they work in specific ways, which you need to understand, to be able to tackle the condition long term. Just viewing it under general IR will not allow you to address it fully.